Study on the inhibition of compound salvia miltiorrhiza on the proliferation of ovarian cancer cells and its preliminary mechanism
10.12092/j.issn.1009-2501.2022.05.005
- Author:
Zhaoya DENG
1
;
Yan LI
1
;
Jian LIU
1
;
Yinjiu HUANG
2
Author Information
1. First Affiliated Hospital of Bengbu Medical College
2. School of Life Sciences of Bengbu Medical College
- Publication Type:Journal Article
- Keywords:
Compound salvia miltiorrhiza;
Luteolin;
Ovarian cancer
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2022;27(5):526-534
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the inhibitory effect and mechanism of compound salvia miltiorrhiza on ovarian cancer by using network pharmacology and molecular docking knowledge. METHODS: The core components of compound salvia miltiorrhiza and the inhibitory effect of compound salvia miltiorrhiza on ovarian cancer cell cycle were studied by combining the methods of MTT cell cycle inhibition and MTT signal network of compound salvia miltiorrhiza. RESULTS: Based on network pharmacology, the core components of compound salvia miltiorrhiza were luteolin and quercetin, and the core target of the disease was VEGFA, SRC, EGFR, hsp90aa1. The docking mode between the core component and the core target EGFR was verified and analyzed by molecular docking. Finally, MTT colorimetry was used to verify that luteolin, one of the core components, significantly inhibited the proliferation of ovarian cancer cells. The results of flow cytometry showed that luteolin induced ovarian cancer A2780 cell cycle arrest in G1/S phase.CONCLUSION: Compound salvia miltiorrhiza preparation can inhibit the proliferation of ovarian cancer cells, which may be related to PI3K Akt signal pathway mediated by EGFR; Network pharmacology and molecular docking technology have important predictability and possibility for the treatment of tumor by compound salvia miltiorrhiza, and have guiding significance for the role and mechanism of compound salvia miltiorrhiza against ovarian cancer cells.